REVIEW

International Journal of Surgery 12 (2014) 113e119

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International Journal of Surgery

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Review

Benefits and risks of splenectomy

Elroy P. Weledji*
Department of Surgery, Faculty of Health Sciences, University of Buea, PO Box 126, Limbe, Cameroon

a r t i c l e i n f o a b s t r a c t

Article history: Splenectomy is a powerful therapeutic procedure in a wide variety of medical disorders provided that it
Received 15 August 2013 is not undertaken lightly and the risks are weighed against the potential benefits in each individual case.
Received in revised form Most of this risk seems to be due to the underlying splenectomy indication and not to splenectomy alone.
27 October 2013
There has been an increased tendency in recent years towards splenic preservation to prevent not only
Accepted 24 November 2013
Available online 3 December 2013
the risk of subsequent overwhelming post-splenectomy infection (OPSI) but the long term risk of car-
diovascular complications. As there is no condition that can be cured by splenectomy, this paper
reviewed the rationale behind the indications for, and the associated risks.
Keywords:
Splenectomy
Method: Electronic searches of the medline (PubMed) database, Cochrane library, and science citation
Indications index were performed to identify original published studies on splenectomy. Relevant articles were
Absolute searched from relevant chapters in specialized texts and all included.
Relative Ó 2013 Surgical Associates Ltd. Published by Elsevier Ltd. All rights reserved.
Hazards

1. Introduction
Since the first deliberate removal of a diseased spleen by Quit-
tenbaum in 1826 splenectomy has become a well established sur-
gical procedure.1 A spleenless existence was considered to be quite
safe as the spleen was considered unnecessary for life until 1952
when King and Schumacher drew attention to the risk of over-
whelming post splenectomy infection (OPSI).2 Since that time
enthusiasm for splenectomy has diminished. The spleen clearly
serves extremely important haematological and immunological
functions. As part of the reticulo-endothelial system and by
receiving 25% of the cardiac output, it plays a major part in the im-
mediate immunological response to blood-borne antigens akin to
the phagocytic role of ‘Kupffer’ cells of the liver in the portal circu-
lation.3 As the spleen is responsible for making antibodies and
removing bacteria, aged, antibody-coated and damaged blood cells,
those without a spleen have an impaired immune system.4,5 Because
of this, splenectomized patients have a more difficult time recov-
ering from pneumonia, meningitis, haemophilus influenzae (Hib)
flu, sepsis, nosocomial infections, babesiosis (a tick-borne disease),
malaria and other parasitic diseases and gram-negative bacterial
diseases from animal bites.6e8 Although the liver can perform this
function in the absence of the spleen, higher levels of specific anti-
body and an intact complement system are probably required.5 As
* Tel.: þ237 99922144.
E-mail address: elroypat@yahoo.co.uk.
the spleen also destroys and modifies abnormal red cells, sequesters
30e40% of the circulating platelet pool and plays a role in the
regulation of plasma volume, the spleen is usually involved in hae-
matological disorders.9,10 Infact, the most frequent medical indica-
tion for splenectomy is a haematologic disorder.11 Overwhelming
bacterial sepsis as a complication in persons with asplenia, is now
infrequent because of pneumococcal vaccinations, prophylactic
penicillin, and prompt medical attention at the first sign of fever.12,13
However, during the past decade evidence has emerged that an
increased risk of thrombosis, both venous and arterial, may result
from splenectomy.14 The increased risk of venous thromboembolism
is particularly within the splenoportal system. This complication has
been described in diverse asplenic states including hereditary
spherocytosis (HS), thalassaemia, other haemolytic anaemias, and
trauma.14e16 In thalassaemia and sickle cell disease, another vascular
complication, pulmonary hypertension (PH), has also been
described following splenectomy, with some studies reporting PH
prevalence as high as 75%.17,18
Splenectomy may have an impact on immunological function
but there is no increased cancer risk among patients splenectom-
ized because of trauma.1 A recent study revealed an increased risk
for some specific cancer sites in patients who underwent splenec-
tomy for non-traumatic reasons, although the effect of treatments
for the underlying disease and lifestyle habits such as cigarette
smoking could not be ruled out in explaining these excess risks.19
In most institutions, trauma is the primary indication for sple-
nectomy, although it is becoming less common in recent years with
more non-operative management of splenic injury.20

1743-9191/$ e see front matter Ó 2013 Surgical Associates Ltd. Published by Elsevier Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.ijsu.2013.11.017
 REVIEW
114 E.P. Weledji / International Journal of Surgery 12 (2014) 113e119
2. Role of the spleen in haematological disorders
The normal spleen may serve as a major site of destruction of
abnormal cellular elements of the blood, e.g. in hereditary spher-
ocytosis, autoimmune anaemia, neutropenia and thrombocyto-
paenia. In the last two situations the spleen serves as the major site
of antibody production. The abnormal or diseased spleen gives rise
to two major syndromes; hypersplenism and symptomatic
splenomegaly. Hypersplenism refers to anaemia, neutropenia and/
or thrombocytopaenia arising singly or in combination as a direct
result of enlargement from whatever cause of the spleen. The
diagnosis is confirmed retrospectively by correction of the cyto-
penia after splenectomy.1,9 Hypersplenic thrombocytopaenia re-
sults largely from increased platelet pooling within the spleen. As
many as 98% of total blood platelets may be sequestered in an
enlarged spleen and there is some evidence that splenomegaly
shortens platelet survival.10,11 The neutropenia of hypersplenism
probably results purely from an increased margination pool of
granulocytes in the vessels of the enlarged spleen. Hypersplenism
often also occurs in conditions that result in bone marrow failure.
Extramedullary haematopoiesis may occur in the inherited hae-
molytic anaemias which soon leads to hepatosplenomegaly and
bone expansion.9 Symptomatic splenomegaly is most commonly
encountered in lymphoproliferative and myeloproliferative disor-
ders. Increased metabolism may give rise to weight loss, fever,
hyperhidrosis, and vague left upper quadrant pain associated with
reduced blood flow and resulting infarction.21
3. Indications for splenectomy
3.1. Absolute indications
The absolute indications include ruptured spleen, treatment of
splenic cysts and abscesses as all organ is usually affected, and
tumour resection involving adjacent organs (Table 1).1,9,22
It can be very difficult to decide whether a patient needs an
emergency splenectomy after trauma, particularly when the pa-
tient is haemodynamically stable and has minimal signs of
abdominal injury. Special investigations do not provide absolute
answers and the risk of delayed and unnecessary laparotomies will
remain. Focused assessment with sonography for trauma (FAST) is
an excellent investigation for haemoperitoneum in blunt trauma
with a sensitivity of 88%.23 An emergency laparotomy is indicated
for a positive FAST in the shocked patient. A CT scan with intrave-
nous contrast is the single most useful investigation in the hae-
modynamically stable patient as it can assess for intraperitoneal
fluid, solid organ injury and retroperitoneal haematoma. Repeated
scanning (ultrasound or CT) have been found particularly helpful in
assessing splenic bleeding or haematoma especially if patient is
slowly dropping her haemoglobin.24e26 Laparoscopy has no role in
trauma (Table 2).24
Table 1
Absolute indications for splenectomy.
Splenic trauma
Splenic rupture
Spontaneous (tropical splenomegaly)
 Delayed rupture (subcapsular haematoma from trauma)
Splenic abscess (e.g. tuberculous infection)
Splenic cysts
Neoplasm
 As part of radical surgical oncological clearance of adjacent tumour. e.g.
locally advanced gastric carcinoma, pancreatic carcinoma
 Angioma
 Primary (rare)
Aneurysm of splenic artery
Table 2
Grading of splenic injury e spleen injury SCALE (1994 Revision).24
Grade Injury type Description of injury
I Haematoma Subcapsular, <10%
Laceration Capsular tear, <1 cm parenchymal depth
II Haematoma Subcapsular, 10e15%, intra parenchymal, <5 cm d
Laceration Capsular tear, 1e3 cm parenchymal depth, trabecular
vessel not involved
III Haematoma Subcapsular, >50% or expanding, ruptured subcapsular or
parenchymal haematoma, intra parenchymal
haematoma >5 cm or expanding
Laceration >3 cm parenchymal depth or involving trabecular vessels
IV Laceration Involving segmental or hilar vessels producing major
devascularisation (>25%)
V Laceration Completely shattered spleen
Hilar vascular injury with devascularised spleen
❖ Advance one grade for multiple injuries up to Grade III.
Because the risks of uncontrolled haemorrhage and major
transfusion are greater than OPSI, splenectomy should be performed
without delay if splenic bleeding is not controlled during laparot-
omy. However, if a splenic tear is found which is not actively bleeding
with adherent clot it should be left undisturbed.22,24,25 The growing
awareness of possible long term complications and the increasing
reports of the failure of prophylactic measures have led increasingly
to the use of partial splenectomy with retention of some splenic
tissue wherever possible, especially in children following splenic
trauma.26,27 Splenic salvage techniques are more feasible in children
because of the greater ratio of splenic capsular tissue to pulp tissue.
They include partial splenectomy, splenorrhaphy, ligation of
segmental vessels and capsular repair.1,28 Partial splenectomy may
be considered with deep tears to the hilum but should only be per-
formed if there are no other life-threatening injuries as it is a
complicated surgery.26,28 Thus, the conservative thing to do in
splenic trauma is splenectomy and it is prudent to err on the side of
splenectomy in all major multiple trauma and military cases.24,25
Superficial splenic tears may be sutured using absorbable mattress
sutures buttressed with Surgicel, teflon or omentum. Ligation of
segmental vessels at the splenic hilum may be useful in obtaining
haemostasis from a splenic tear. Topical haemostatic agents e.g.
microfibrillar collagen (fibrin glue) and absorbable envelopes have
also been used successfully to preserve the spleen.1,28 Splenosis and
auto transplantation may have some minor immunological function
but have not been shown to be effective in preventing overwhelming
post splenectomy infection.27 It seems likely that the normal splenic
vasculature is crucial for maximum protection. Indeed there has
been some uncertainty of the level of splenic function achieved by
partial splenectomy especially if more than half the spleen is
removed or the splenic artery has to be tied as the patient probably
loses most immunological benefit.3 It would be prudent to institute
similar prophylactic measures in these patients to prevent infection
as for asplenic individuals.29
3.1.1. Non-operative management
The current management of trauma is usually dictated by the age
of the patient, the experience of the institution, the individual sur-
geon and the type of trauma.1 Non-operative management of splenic
trauma has also become an option. 20e40% of laparotomies per-
formed for haemoperitoneum reveal that bleeding has stopped and
that the injuries do not require surgery.20 The practice began in the
1970’s in paediatric patients and was highly successful with an
average failure rate of 10.8%. The majority of failures occurring in the
first 24 h.30 In an isolated splenic trauma in a haemodynamically
stable patient with no evidence of continuous bleeding, regular ob-
servations and haemoglobin measurements may be suitable for at
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E.P. Weledji / International Journal of Surgery 12 (2014) 113e119 115

least 10days.1,24 The patient should be counselled on the risk of
delayed rupture after a period of several days (or even of 2e3 weeks).
This equally dangerous condition may arise when the damage to the
spleen is less severe. The laceration may become temporarily sealed
eoff by omentum or by blood clot or the bleeding may at first be
confined within the capsule of the organ (subcapsular).22 A patient
under non-operative management for blunt abdominal injuries
should be admitted initially to ICU/HDU for at least 48e72 h for close
monitoring of vital signs, repeated clinical examinations and follow-
up investigations as indicated. But splenectomy or splenic repair is
warranted in an unstable patient despite resuscitation.31 Arteriog-
raphy with embolisation are increasingly important adjuncts to non-
operative management of splenic injuries.20,28
3.2. Relative indications for splenectomy
The relative indications for splenectomy includes hyper-
splenism, symptomatic splenomegaly and destruction of abnormal
blood cells in the spleen.1,9 Splenectomy is performed in patients
having haemolytic anaemia (e.g., hereditary spherocytosis [HS],
and autoimmune haemolytic anaemia) because the intrinsically
abnormal or antibody-coated red blood cells are prematurely
destroyed by splenic macrophages (Table 3). Because splenectomy
can ameliorate the underlying anaemia, it is often considered the
treatment of choice although none of these conditions can be cured
by splenectomy. Two facts must be established before splenectomy
in haematological patients. Firstly, the spleen must be shown to be
the site of excessive destruction of red cells, by examination of the
bone marrow and of peripheral blood and isotope studies to illus-
trate excessive uptake in the spleen. Secondly, the bone marrow
must be shown capable of producing sufficient new cells to correct
the cytopenia in the absence of the spleen. Otherwise, no reversal
of cytopenia is possible and the patient’s condition will continue to
deteriorate.1 Where splenectomy is being carried out for haema-
tological disorders a careful search should be also be made for
accessory spleens.9
The long-term thromboembolic risk which is higher in haema-
tological disorders associated with ongoing haemolysis, particu-
larly thalassaemia intermedia, has led to a more non-operative
approach.14 In comparison, patients with ITP appear to be at
lower risk of adverse effects of splenectomy, which maintains its
place as the potentially most curative and safe second-line treat-
ment. However, a splenectomy-sparing approach is also emerging
for ITP, and recent guidelines recommend that this procedure is
deferred until 12 months following ITP diagnosis, to allow sufficient
time for possible remission.32
3.2.1. Red cell disorders
Red cell disorders including hereditary spherocytosis, ellipto-
cytosis, pyruvate kinase deficiency present with severe anaemia,
haemolytic crisis, chronic leg ulcers and sometimes pigment gall-
stones in the former.9 Splenectomy reliably corrects the clinical
picture with very low mortality and morbidity, but is usually
delayed beyond five years of age to reduce the risk of overwhelming
post splenectomy infection.33 Cholecystectomy is done if there is
associated gallstone disease.1,9

Table 3 3.2.2. Thalassaemia syndromes

Relative indications and benefits of splenectomy.11 Thalassaemia syndromes are inherited disorders in which the
Condition Degree of Indications for rate of synthesis of one or more globin chain are reduced resulting
splenomegalya splenectomyb in defective erythropoiesis, haemolysis and consequent marked
1. Blood and reticuloendothelial disease splenomegaly and hypersplenism with increasing transfusion re-
a) Haemolytic quirements and severe iron overload. Splenectomy reduces the
i. Congenital haemolytic anaemia D DDD need for blood transfusion requirements and it is usually done
ii. Acquired haemolytic anaemia DD DD before six and eight years.9,14 As the risk of thrombotic complica-
iii. Thalassaemia D D
b) Haematological malignancy
tions and sequelae (venous thrombosis and pulmonary hyperten-
i. Acute leukaemia D 0 sion) arising after an average interval of about 8 years is particularly
ii. Chronic myeloid leukaemia DDD D prominent in patients who underwent splenectomy, the current
iii. Chronic lymphatic leukaemia DD D thrust in prevention is to avoid splenectomy, even if this choice
iv. Lymphoma (Hodgkin’s) D D
entails a greater need of red cell transfusion and iron chelation. It
c) Myeloproliferative disorders
i. Polycythaemia vera DD 0 has also been shown that in splenectomized patients with thalas-
ii. Myeloid metaplasia (myelofibrosis) DDD D saemia intermedia who developed thrombosis, the platelet count
d) Thrombocytopaenic disorders was much higher than in those who did not in spite of being
i. Acute ITP þ D asplenic. Although it remains to be established whether or not the
ii. Chronic ITP DD DDD
2. Infective and inflammatory
high platelet count is the cause of thrombosis, it is reasonable to
a) Parasites (hydatid) DD DDD recommend aspirin (100e300 mg daily) to patients at higher risk
b) Protozoal (malaria) DDD D because of a high platelet count.15
c) Inflammatory (Felty’s syndrome) DD D
3. Neoplastic
3.2.3. Homozygous sickle cell disease
a) Angioma þþ 0
b) Cysts DD DDD Homozygous sickle cell disease is characterized by chronic
c) Metastases D 0 haemolysis and recurrent episodes of tissue infarction. Repeated
4. Cryptogenic splenic infarction usually causes ‘autosplenectomy’ before adult-
a) Tropical splenomegaly DDD D hood, but splenectomy may occasionally be required for persistent
b) Non-tropical splenomegaly DDD DDD
5. Congestive
hypersplenism.8 Acute splenic sequestration is the second most
a) Portal hypertension common cause of death in the first decade of life and has a high rate
i. Intrahepatic D D of recurrence.34 Splenectomy may thus be indicated for infants
ii. Extrahepatic DD D with recurrent acute splenic sequestration characterized by rapidly
6. Metabolic storage disorders
falling haemoglobin due to pooling of blood in an acutely enlarged
a) Amyloidosis þþ 0
b) Gaucher’s disease DDD D spleen.35 Patients who have a severe episode of acute splenic
a
sequestration and are below age 2 years should be placed in a
Degree of splenomegaly: þþþ ¼ marked (below umbilicus); þþ ¼ moderate
(4e8 cm below costal margin); þ ¼ slight (4 cm ejust palpable).
chronic transfusion programme to keep HbS level below 30% until a
b
Indications for splenectomy: þþþ ¼ benefited by splenectomy; þþ ¼ often splenectomy is performed at age 2 years.36 Splenectomy, if full, will
benefited by splenectomy; þ ¼ splenectomy sometimes indicated. prevent further sequestration and if partial, may reduce the
 REVIEW
116 E.P. Weledji / International Journal of Surgery 12 (2014) 113e119
recurrence of acute splenic sequestration crises. However, there is a
lack of evidence from trials showing that splenectomy improves
survival and decreases morbidity in people with sickle cell disease.
There is a need for a well-designed, adequately-powered, ran-
domized controlled trial to assess the benefits and risks of sple-
nectomy compared to transfusion programmes, as a means of
improving survival and decreasing mortality from acute splenic
sequestration in people with sickle cell disease.35 Infection is still
the commonest cause of death irrespective of splenectomy.34e36
3.2.4. Platelet disorders
Splenectomies have been used to treat immune thrombocyto-
penic purpura (ITP) since 1913.9,37 However its long-term safety is
not well elucidated.32,38,39 In ITP the spleen plays a dual role,
serving as the main site of both antiplatelet antibody production
and destruction of antibody-coated platelets. Therefore removing
the spleen may reduce the amount of anti-platelet antibodies in
addition to removing the antibody-coated platelets. While a sple-
nectomy may raise the platelet count, it does not eliminate ITP
since the antibody-coated platelets remain in circulation.38
Although the spleen is often the major site of antibody-coated
platelet destruction, platelets may also be removed from circula-
tion by the liver, by a combination of the spleen and liver, or within
the blood stream. Therefore, splenectomies are not always suc-
cessful in raising the platelet count and may fail over time,
prompting a return of low platelets. The sequestration site is a good
predictive element in the short-term efficacy of splenectomy with a
platelet count exceeding 100  109/l if splenic sequestration
occurred alone but much less with mixed and least with hepatic
sequestration.38,39 Splenectomy is indicated following failed
response to steroid treatment and about 70% achieve an immediate
and sustained platelet response after splenectomy but 7% achieve a
delayed response. All accessory spleens must be sought and
removed. If the platelet count is less than 70,000 pre-operatively
then fresh platelets are given once the splenic artery is clamped
otherwise they are “consumed” in a few minutes by the unclamped
spleen. For those who do respond, 30e35% relapse over time.1,9,32
Previous response to corticosteroids or other treatments are not
very good predictors of splenectomy success. Age under 40 years is
the only positive predictive factor for the long term response to
splenectomy in ITP.40 Researchers suggest that a raised serum
biomarker protein haptoglobin (Hp) that binds to free haemoglobin
released by red blood cells predicts long-term response to sple-
nectomy for ITP in about 80% of cases.41 In a small proportion of the
splenectomized ITP population a second surgery is occasionally
required to remove an (extra)accessory spleen if the patient has
relapsed following a successful first surgery. The first meta-analysis
of randomized clinical trials and observational studies on rituximab
has shown its effectiveness as a splenectomy-avoiding option in
adult chronic ITP. Age was also the most relevant effect and ritux-
imab should be used earlier in non-splenectomised patients.42
Laparoscopic splenectomy (LS) is preferred when possible in ITP
as these patients are on steroids with risk of infection and poor
wound healing.43 A recent retrospective study demonstrated a 6.4%
conversion rate to open surgery which was mostly due to larger
spleens.44 A previous comparative study on operations on massive
splenomegaly had demonstrated a 6.6% conversion rate to open
and despite a significant longer operating time, the post operative
recovery following laparoscopic splenectomy was smoother with
lower morbidity and shorter post operative hospital stay.45
3.2.5. Lymphoproliferative disease (Hodgkin’s/Non-Hodgkin’s
lymphoma)
Clinical studies have not demonstrated an improvement in
prognosis following splenectomy and the indications are
diminishing with the effectiveness of CT scanning in staging Hodg-
kin’s disease and the responsiveness to chemotherapy.21 Splenec-
tomy, may on occasion be required to make a positive diagnosis
because of the suspicion of an underlying lymphoma, reticulosis or
infiltrative condition. Several investigations have suggested that
splenectomy in patients with Hodgkin’s disease increases the risk for
secondary leukaemia independent of treatment.19
3.2.6. Myelofibrosis
Splenectomy for myelofibrosis does not prolong survival but may
be indicated as a palliative measure for symptomatic splenomegaly.1
The proliferative process affect the bone marrow, liver, spleen and
lymph nodes. The spleen may be grossly enlarged and portal hy-
pertension may develop. Early post operative morbidity and mor-
tality are very high due to impaired haemostasis, large spleen and
the usually elderly patients in poor general condition.46 Splenec-
tomy should be performed very occasionally for severe pain and
hypersplenism (low haemoglobin and low white blood cell count) at
an earlier stage of the disease. Otherwise conservative treatment
with blood transfusion for anaemia may give better palliation.47
3.2.7. Malaria
Comparison of infected patients with or without spleens sup-
ports the idea that the spleen removes dead or damaged intracel-
lular parasites and returns intact erythrocytes into the blood
stream.7,48 Splenectomy is therefore not indicated for symptomatic
splenomegaly unless the spleen has ruptured.22
3.2.8. Congestive splenomegaly
Congestive splenomegaly from intrahepatic or extrahepatic
portal venous obstruction is most commonly caused by cirrhosis.
Splenectomy is reserved for the rare patient with severe residual
thrombocytopaenia after portasystemic shunting.49 If splenic
venous thrombosis is the underlying cause then splenectomy is the
treatment of choice.1,9
3.2.9. Felty’s syndrome
Felty’s syndrome is characterized by rheumatoid arthritis and
splenic neutropenia, commonly associated with anaemia and
chronic leg ulcers. Many immunological and rheumatological dis-
orders are associated with impairment of the spleen’s phagocytic
and immunological functions. Transient functional hyposplenism
may also occur during therapy with corticosteroids and after
pharmaceutical reticulo-endothelial blockade with intravenous IgG
or anti-D immunoglobulin. Splenectomy controls the neutropenia
in the majority of patients with serious or recurrent infections or
non healing leg ulcers.50
4. Hazards of splenectomy
The complications of splenectomy may be conveniently divided
into acute, short and long term as shown in Table 4.
4.1. Haemorrhage
During operation bleeding can occur from divided adhesions, a
tear in the splenic capsule, from the splenic vessels or short gastrics or
from the tail of the pancreas. After operation, reactive haemorrhage
may occur from the small vessels in the posterior abdominal wall and
diaphragm. Therefore haemostasis must be meticulous to prevent the
development of a large haematoma, which may become infected. The
operative mortality varies between 3 and 15%, depending upon the
physical state of the patient and the condition for which the operation
was performed.1 The mortality is particularly high (30%) following
splenectomy for myeloproliferative disorders (i.e. myelofibrosis,
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E.P. Weledji / International Journal of Surgery 12 (2014) 113e119 117

Table 4 of prophylactic anticoagulation which usually follow local institu-

Complications of splenectomy.
Acute
Haemorrhage
 During
 Immediately after
Pulmonary atelectasis
and pneumonia
Sympathetic pleural
effusion
Subphrenic
abscess/cellulitis
Gastric ileus
Acute pancreatitis
Thrombocytosis
and leucocytosis
(peaks 7the14th day)
Severe thrombosis
after splenectomy for
myeloproliferative disorders
tional protocols. Post operative antithrombotic prophylaxis ranged
Short term Long term from no prophylaxis to heparin for seven days or longer.53 Treat-
Overwhelming postoperative OPSI þ/ DIC
ment of symptomatic splenic vein thrombosis with heparin and
infection (OPSI) þ/ warfarin leads to complete resolution of thrombosis in 67%, to
disseminated partial resolution in 13%, but persistent occlusion, portal hyper-
intravascular coagulation tension or cavernoma occurred in 20%.54 The long-term outcome of
(DIC)
treatment failures is unknown. Well-designed randomized studies
Pulmonary infection Pulmonary
infection on the prophylaxis of venous thromboembolism after splenectomy
Deep vein thrombosis Venous are urgently needed.
thrombosis
4.3. Subphrenic abscess
Spleno-portal thrombosis Pulmonary
(fever, abdominal hypertension Subphrenic abscess is not common. It may arise from an infected
complaints) haematoma or infection following injury of the adjacent stomach
Enhanced or colon. Patients with autoimmune disorders e.g. immune
atherosclerosis
thrombocytopenic purpura (ITP) who have been on steroids have a
Arterial
thrombosis high frequency of subphrenic abscesses and are mostly aborted by a
course of antibiotics.47
4.4. Chest infection

The patients with lymphoproliferative malignancies e.g. Hodg-

47 kin’s lymphoma, chronic lymphocytic leukaemia have a high
chronic granulocytic leukaemia). The high morbidity and mortality
morbidity from infective complications especially bronchitis and
are as a result of bleeding. The platelets in myeloproliferative disor-
pneumonia.6,21,47 By being minimally invasive with less pain, the
ders are a part of the malignant population and defects in function
laparoscopic technique as opposed to open may decrease the risk of
have been reported. Therefore the assessment of platelet function or
post operative chest infections due to atelectasis and sputum
bleeding time should be performed before splenectomy in this group
retention.45
and the possibility of platelet transfusion despite a normal platelet
count should be considered.46,47 Patients over 65 have a higher
4.5. OPSI
complication and fatality rate.46

The major long-term risk of splenectomy is overwhelming post-

4.2. Thromboembolic
Thromboembolic complications following splenectomy for
haematological diseases occur in up to 10% of patients and may
range from portal vein thrombosis to pulmonary embolism and
deep vein thrombosis.51 Given the increased platelet count post-
splenectomy which is maximal by the 10th day, deep vein throm-
bosis (DVT) or pulmonary embolism has also to be considered as a
cause of post operative pyrexia. Both DVT and small pulmonary
embolism may otherwise be silent although they may of course be
the harbinger of a massive pulmonary embolism.52 Splenic/portal
vein thrombosis is an alarming complication of splenectomy pre-
senting with fever and abdominal pain and a mortality of w10%.51e
54
The median time from splenectomy to symptomatic splenic vein
thrombosis is 8e12 days.52 Fatal outcomes have been reported 7e
35 days after splenectomy for autoimmune haemolytic anaemia,
immune thrombocytopaenia and indolent lymphoma respec-
tively.53 Retrospective studies have shown the incidence of symp-
tomatic splenic/portal vein thrombosis varying from 0.7% to 8%.53,54
The overall risk addressed in prospective and retrospective ran-
domized or non-randomized trials is 3.3%. Risk factors are big
spleens (i.e. myeloproloferative disorders and hereditary haemo-
lytic anaemia) whereas risk is low in autoimmune thrombocyto-
paenia and trauma. The incidence is approximately the same in
laparoscopic and open splenectomy.54 A high index of suspicion,
early diagnosis by contrast eenhanced computed tomography and
prompt anticoagulation are key to successful outcome.54 Generally
prior to splenectomy, correction of preoperative coagulation ab-
normalities, intensive post operative chest physiotherapy and an-
tiplatelet therapy with low dose aspirin if platelet counts rise
postoperatively above 800  109/l all make surgery safer.1 There
exist no standard recommendations for the duration and intensity
splenectomy infection (OPSI).2 Post trauma, the life-time risk of
OPSI is 0.1e0.5% and has a mortality of up to 50%.12 The risk of
infection is life long as cases of fulminant infection have been re-
ported more than 20 years post splenectomy and is greater with
encapsulated organisms -streptococcus pneumonia, nessieria
meningitides, and H influenza.29,55 Pneumococcal infection is most
common and carries a mortality rate of up to 60%.2,12 Infection with
H influenza type B, whilst much less common is nonetheless sig-
nificant, particularly in children. The risk of OPSI is greatest during
the first 3- years post splenectomy; greater in children especially
under 5 years and who have had splenectomy for trauma (>10%
excess risk) than adults (<1%).2,29,56 The risk of infection with
encapsulated organisms is increased in immunosuppressed or
immunodeficient individuals (e.g. HIV, myeloma, leukaemia).29,57
5. Prevention of overwhelming post splenectomy infection
(OPSI)
Overwhelming infection in hyposplenic or asplenic patients
thus remains an area of concern.2,12 This may include infection by
unusual serotypes not included in the vaccinations.62,63 All sple-
nectomized patients greater than 2 yrs old and those with func-
tional hyposplenism should receive pneumococcal vaccination,
haemophilus influenzae type b conjugate vaccine and meningo-
coccal conjugate vaccine at least 2 weeks before splenectomy in
order to ensure an optimal antibody response. Immunisation
should be administered following emergency splenectomy, but the
effect is not as good, although still better than not being given.29
Time frames may be different for those with immunosuppressive,
sickle-cell disorders and on immune suppressing therapies.29
Because of waning immunity timing of revaccination may be
determined by levels of protective antibody (Table 5).29,58,64
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118 E.P. Weledji / International Journal of Surgery 12 (2014) 113e119

Table 5
Summary of British haematology guidelines on timing and type of vaccinations in elective and emergency splenectomy.29

Class OPSI prophylaxis Timing

 <2yrs  None (immature immune system)

 >2yrs  Immunization  At least 2 weeks before splenectomy for
 Functional hyposplenism optimal antibody response
(e.g. sickle cell, ITP, coeliac dis)
 Emergency splenectomy  Immunization Following emergency splenectomy
 Immunization effect not as good
 Still better than not being given
 Asplenic patients  Immunization
 Add influenza vaccine (prophylaxis against
secondary bacterial infection)9
 Splenectomy in underlying immunosuppressive  Immunization  Monitor response to pneumococcal vaccination
disease (e.g. lymphoproliferative) or  Life-long prophylactic antibiotics  Timing of revaccination determine by levels of
sickle-cell disorder37 protective antibody
 Splenectomy in patients on immune Immunization  Immunization delayed at least 6 months following
suppressing therapies (chemotherapy  Life-long prophylactic antibiotics chemo/radiotherapy
and/or radiotherapy)
 High risk patients (<18 yrs, immunosuppressed)  Life-long oral prophylactic antibiotics against Regularly reviewed in light of local pneumococcal
pneumococcal infection (penicillins/macrolides) resistance patterns
 Prompt systemic antibiotic treatment for infection
 Low risk patients  Counselled on risks and benefits of life-long
antibiotics and may choose to discontinue
 Carry a supply of appropriate antibiotics for emergency
 Malaria belt  Antimalarial prophylaxis
 Treat malaria infection early and aggressively

6. Discussion cured by splenectomy. The spleen is however simply an enlarged

Regardless of indication, the adjusted short- and long-term risk
of death for splenectomised patients was higher than the general
population. Within 90 days post-splenectomy, the adjusted relative
risk (RR) for death was 33.6%.59 This risk declined substantially after
90 days post-splenectomy but remained higher 365 days post-
splenectomy for all indications compared to the general popula-
tion.59 This may suggest that the indication for splenectomy is the
determinant factor on outcome. The best prognosis being with
splenectomy for trauma than for an associated disease process.60
This is also in line with the observation that the ability of an
asplenic individual to mount an adequate protective antibody
response may relate more to the indication for, or age at, splenec-
tomy, and to the presence of underlying immune suppression than
the absence of the spleen.61
With the largely significant success of prophylactic measures to
prevent OPSI, other complications of asplenia are surfacing.14e18,65
The compelling evidence for a hypercoagulable state after splenec-
tomy performed for various indications is probably compounded by
other underlying conditions, especially intravascular haemolysis as
seen in thalassaemia and sickle cell disease14 Recent observations
suggest that asplenia may be a risk factor for pulmonary hypertension
irrespective of the underlying condition.15 Although there is sub-
stantial evidence that pulmonary hypertension and venous throm-
bosis occur at increased rates in asplenic hosts, the strength of
evidence is less convincing with atherothrombosis causing dementia,
myocardial infarction and stroke. However, the observed memory
disturbances due to ischaemic small vessel disease associated with
platelet disorders following splenectomy warrants further investi-
gation.66 Thus, vascular events after splenectomy are likely to be
multifactorial. It may result from some combination of hypercoagu-
lability, platelet activation, disturbance and activation of the endo-
thelium, and altered lipid profiles.67 Absence of this extremely
sensitive filter function of the spleen may permit particulate matter
and damaged cells to persist in the blood stream, thereby perturbing
and activating the vascular endothelium leading to a shift in vascular
homeostasis toward enhanced coagulation. Unfortunately, despite
these risks alongside the potential benefits no condition is actually
lymph node.
7. Conclusions
The spleen, whether anatomically and physiologically normal or
diseased, may significantly worsen the clinical picture in a variety of
medical disorders. However, splenectomy should be undertaken only
after careful balancing of the short and long term risks and potential
benefits to the patient. Most of this risk seems to be due to the un-
derlying splenectomy indication and not to splenectomy alone.
Ethical approval
Not required.
Funding
Ministry of Higher Education in Cameroon.
Author contribution
Dr E.P. Weledji is sole author.
Conflict of interest
None.
References
1. Clarke PJ, Morris PJ. Surgery of the spleen. In: Oxford textbook of Surgery, vol. 2.
Morris and Matt Oxford University Press; 1994.
2. King H, Schummacher HB. Splenic studies: 1. Susceptibility to infection after
splenectomy performed in infancy. Ann Surg 1952;136:704e6.
3. Traub A, Giebink GS, Smith C, et al. Splenic reticuloendothelial function after
splenectomy, spleen repair and spleen autotransplantation. N Engl J Med
1987;317:1559e64.
4. Rosse WF. The spleen as a filter. N Engl J Med 1987;317:704e6.
5. Hosea SW, Brown EJ, Hamburger MI, Frank MM. Opsonic requirements for
intravascular clearance after splenectomy. N Engl J Med 1981;304:246e50.
6. Thomsen RW, Schooren WM, Farkas DK, et al. Risk for hospital contact with
infection in patients with splenectomy: a population-based cohort study. Ann
Intern Med 2009;151(8):546e55. 20.
7. Shute PG. Splenectomy and susceptibility to malaria and babesiae infection.
BMJ 1975;I:516.
 REVIEW
E.P. Weledji / International Journal of Surgery 12 (2014) 113e119
8. Teo KG, Anavekar NS, Yazdabadi A, Ricketts S. Asplenic fulminant sepsis sec-
ondary to a dog bite complicated by toxic epidermal necrolysis/Stevemse
Johnson syndrome. N Z Med J 2012;125:74e7.
9. Lewis SM, Swirsk D. The spleen and its disorders. In: Weatherall D,
Ledingham JG, Warrel DA, editors. Oxford textbook of Medicine, vol. 3; 1996.
10. Aster RH. Pooling of platelets in the spleen: the role in the pathogenesis of
‘hypersplenic’ thrombocytopenia. J Clin Invest 1966;45:645e57.
11. Coon WW. Splenectomy for splenomegaly and secondary hypersplenism.
World J Surg 1985;0:437e43.
12. Sarangi J, Coleby M, Trivella M, Reilly S. Prevention of post splenectomy sepsis:
a population based approach. J Public Health Med 1997;19(2):208e12.
13. Zarachi MH, Rosner F. Rarity of failure of penicillin prophylaxis to prevent
splenectomy sepsis. Arch Intern Med 1986;140:1207e8.
14. Crary SE, Buchanan GR. Vascular complications following splenectomy for
hematologic disorders. Blood 2009;114:2861e8.
15. Taher A, Isma’eel H, Mehio G, et al. Prevalence of thromboembolic events
among 8,860 patients with thalassaemia major and intermedia in the Medi-
terranean area and Iran. Thromb Haemost 2006;96:488e91.
16. Schilling RF, Gangnon RE, Traver MI. Delayed adverse vascular events after
splenectomy in hereditary spherocytosis. J Thromb Haemost 2008;6:1289e95.
17. Singer ST, Kuypers FA, Styles L, et al. Pulmonary hypertension in thalassemia:
association with platelet activation and hypercoagulable state. Am J Hematol
2006;81:670.
18. Phrommintikul A, Sukonthasarn A, Kanjanavanit R, Nawarawong W. Splenec-
tomy: a strong risk factor for pulmonary hypertension in patients with thal-
assaemia. Heart 2006;92:1467e72.
19. Mellemkjoer L, Olsen JH, Linet MS, et al. Cancer risk after splenectomy. Cancer
1995;75:577e83.
20. Stassen NA, Bhullar I, Cheng J, et al. Selective non-operative management of
blunt splenic injury: an Eastern association for the surgery of trauma practice
management guideline. J Trauma Acute Care Surg 2012;73:294e300.
21. Young AE, Timothy AR. The spleen and lymphoma. In: Barnard, Young, editors.
The new Aird’s companion in surgical studies. 2nd ed. 1998.
22. Cochrane JPS. The spleen-ruptured spleen. Br J Hosp Med 1980;25:398e404.
23. Staren E, editor. Ultrasound for the surgeon. New York: Lippincott Raven; 1996.
24. Botha A, Brooks A, Loosemore T, editors. Definitive surgical trauma skills manual.
The Royal College of Surgeons of England; 2002.
25. Bowley DMG, Barker P, Boffard KD. Damage control surgery e concepts and
practice. JR Army Med Corps 2000;146:176e82.
26. Buyukunal C, Danismend N, Yeker D. Spleen saving procedures in paediatric
splenic trauma. Br J Surg 1987;74:350e2.
27. Rice HM, James PD. Ectopic splenic tissue failed to prevent pneumococcal
septicaemia after splenectomy for trauma. Lancet 1980;1:565e6.
28. Van der Hul RL, van Overhager H, Dallinger RJ, de Graffe PW. Splenic salvage by
superselective embolisation after blunt abdominal trauma. Eur J Surg
2001;167(1):73e5.
29. Davies JM, Lewis MPN, Wimperis J, et al. Guidelines for the prevention and
treatment of infection in patients with an absent or dysfunctional spleen.
Prepared on behalf of the British Committee for standards in Haematology by a
Working Party of the Haematology-Oncology Task force. Br J Haematol
2011;155:308e17.
30. Gheju BM, Venter MR, Marien RC, Smaradicher R. Non-operative management
of splenic trauma. J Med Life 2012;5(1):47e58.
31. Raza M, Aba Y, Deri V, et al. Non-operative management of abdominal trauma
e 10 years review. World J Emerg Surg 2013;8(1):14.
32. Provan D, Stasi R, Newland A, et al. International consensus report on the
investigation and management of primary immune thrombocytopenia. Blood
2010;115:168e86.
33. Coon WW. Splenectomy in the treatment of haemolytic anaemia. Arch Surg
1985;120:625e8.
34. Rezende PV, Viana MB, Mureo M, et al. Acute splenic sequestration in a cohort
of children with sickle cell anaemia. J Pediatr (Rio J) 2009;85(2):163e9.
35. Owusu-Ofuri S, Hirst C. Splenectomy versus conservative management for
acute sequestration crisis in people with sickle cell disease. Cochrane Database
Syst Rev 2013:CD003425. Issue 4.
36. Wright JG, Hermbleton RI, Thomas PW, et al. Post splenectomy course in ho-
mozygous sickle cell disease. J Pediatr 1999;134:304e9. 1999.
37. Coon WW. Splenectomy for idiopathic thrombocytopenic purpura. Surg
Gynecol Obstet 1987;164:225e9.
38. Kojouri K, Vesely SK, Terrell DR, George JN. Splenectomy for adult patients with
idiopathic thrombocytopenic purpura: a systematic review to assess long-term
119
platelet count responses, prediction of response, and surgical complications.
Blood 2004;104(9):2623e34.
39. Najean Y, Dufour VJD, Toubert ME. The site of platelet destruction in throm-
bocytopenic purpura as a predictive index of the efficacy of splenectomy. Br J
Haematol 1992;79:271e6.
40. Zheng CX, Zhuang QJ, Zhang LJ, et al. Proteomics-based identification of
haptoglobin as a favourable serum biomarker for predicting long-term
response to splenectomy in patients with primary immune thrombocyto-
penia. RJ Transl Med. 2012 Oct 7;10(1):208.
41. Fabris F, Tassan T, Ramon R, et al. Age as the major predictive factor of long-
term response to splenectomy in immune thrombocytopenia purpura. Br J
Haematol 2001;112:637e40.
42. Auger S, Duny Y, Rossi JF, Quittet P. Rituximab before splenectomy in adults
with primary idiopathic thrombocytopenic purpura: a meta-analysis. Br J
Haematol 2012;158:386e98.
43. Sotomayor-Ramirez RK. Efficacy and safety of laparoscopic splenectomy: review
of 14 adult cases using the lateral approach. Bol Assoc Med PR 2009;101:43e9.
44. Bulus H, Mahmoud H, Altum H, et al. Outcomes of laparoscopic versus open
splenectomy. J Korean Surg Soc 2013;84:38e42.
45. Owera A, Hamade AM, Bani Hani OI, Ammori BJ. Laparoscopic versus open
splenectomy for massive splenomegaly: a comparative study. J Laparoendosc
Adv Surg Tech A 2006;16:241e6.
46. Jarviness H, Kirvaleaksu E. Splenectomy for myelofibrosis. Ann Clin Res
1982;14:66e71.
47. Malmacus J, Akre T, Adami HO, Hasberg H. Early postoperative course following
elective splenectomy in haematological diseases: a high complication rate in
patients with myeloproliferative disorders. Br J Surg 1986;73:720e3.
48. Chotivanich K, Udomsanngpetch R, McGready R, et al. Central role of the spleen
in malaria parasite clearance. J Infect Dis 2002;185:1538e41.
49. Hutson DG, Zeppa R, Levi JU. The effect of the distal splenorenal shunt on
hypersplenism. Ann Surg 1977;185:605e12.
50. Coon WW. Felty’s syndrome- when splenectomy indicated? Am J Surg
1985;149:272e5.
51. Mohren M, Markmann I, Dworschak U, et al. Thromboembolic complications
after splenectomy for haematologic diseases. Am J Hematol 2004;2004(76):
143e7.
52. Krauth M, Lechner K, Edmund AM, et al. The postoperative splenic/portal
thrombosis after splenectomy and its prevention e an unresolved issue.
Hematologica 2008;93:1227e32.
53. Rattner DW, Ellman L, Warshaw AL. Portal vein thrombosis after elective
splenectomy. An underappreciated, potentially lethal syndrome. Arch Surg
1993;128:565e9. discussion 569e70.
54. Winslow ER, Brunt LM, Drebin JA, Soper NJ, Klingensmith ME. Portal vein
thrombosis after splenectomy. Am J Surg 2002;184:631e6.
55. Frackle EL, Neu HC. Post splenectomy infection. Surg Clin North Am 1981;61:
135e55.
56. Evans D. Postsplenectomy sepsis 10 years or more after operation. J Clin path
1995;38:309e11.
57. Shaw JH, Print CG. Post splenectomy sepsis. Br J Surg 1991;78:1035e8.
58. Weintrub PS, Schffmass G, Adigu JE. Long term follow up and booster immu-
nisation with polyvalent polysaccharide in patients with sickle cell anaemia.
J Pediatr 1984;105:261e3.
59. Yong M, Thomsen RW, Schoonen WM, et al. Mortality risk in splenectom-
ised patients: a Danish population-based cohort study. Eur J Intern Med
2010;21(1):12e6.
60. Robinette CD, Franmer Jr JT. Splenectomy and subsequent mortality in veterans
of the 1939e45 war. Lancet 1977;11:127e9.
61. Holdsworth RJ, Irving AD, Cuscheiri A. Postsplenectomy sepsis and its mortality
rate: actual versus perceived risks. Br J Surg 1991;78:1035e8.
62. Weledji EP. Why’s or when’s of splenectomy. Darlington Postgrad J 2001;21:
46e55.
63. Applebaum PC, Shaikh BS, Widome MD, Gordon RA. Fatal pneumococcal bac-
teraemia in a vaccinated splenectomised child. N Engl J Med 1979;35:203e4.
64. Abildqaard N, Nielsen JL. Pneumococcal septicaemia and meningitis in vacci-
nated splenectomized adult patients. Scand J Infect Dis 1994;26:615e7.
65. Ong EL, Hassan IS, Snow MH. Pneumococcal sepsis in a splenectomized patient.
Br J Gen Pract 1995;45:502e3.
66. Ahn YS, Horshman LL, Jy W, et al. Vascular dementia in patients with immune
thrombocytopenic purpura. Thromb Res 2002;107:337e44.
67. Witztum JL. Splenic immunity and atherosclerosis: a glimpse into a novel
paradigm. J Clin Invest 2002;109:721e4.